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. 2008 Sep;57(9):2413–2420. doi: 10.2337/db07-1323

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Copyright © 2008, American Diabetes Association

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 4. — Prevention of HES-1 upregulation by shRNA reduces replication of cultured human islet cells and eGFP⁺ cells derived from β-cells. A: Immunoblotting for HES-1 in protein extracted from islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. β-Actin served as a loading control. B: Top panel: Incidence of BrdU⁺ cells among cultured islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. Data are means ± SD (n = 3 donors; >1,000 cells counted in culture from each donor; P = 0.02). Bottom panel: Incidence of Ki67⁺ cells among eGFP⁺ cells from two representative donors following infection with HES1 shRNA or nontarget virus. Data are based on >1,000 cells counted in culture from each donor. □, G13; ▪, I10. C: Immunoblotting for PARP in protein extracted from islet cells following infection with nontarget (lane 3) or HES1 shRNA TRCN18993 virus (lane 4). Uninfected cells incubated with (lane 1) or without (lane 2) the apoptotic agent staurosporin served as controls. The lower band in lane 1 represents cleaved PARP. β-Actin served as a loading control. D: qPCR analysis of RNA extracted from islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. RQ indicates relative quantification compared with P0. Data are means ± SD (n = 3 donors). Only the change in p57 is significant (P = 0.001 vs. cells infected with nontarget virus, indicated by star). ▪, P0; □, nontarget;, HES1 shRNA. All the analyses were done 14 days following viral infection.

Inline graphic — Prevention of HES-1 upregulation by shRNA reduces replication of cultured human islet cells and eGFP⁺ cells derived from β-cells. A: Immunoblotting for HES-1 in protein extracted from islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. β-Actin served as a loading control. B: Top panel: Incidence of BrdU⁺ cells among cultured islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. Data are means ± SD (n = 3 donors; >1,000 cells counted in culture from each donor; P = 0.02). Bottom panel: Incidence of Ki67⁺ cells among eGFP⁺ cells from two representative donors following infection with HES1 shRNA or nontarget virus. Data are based on >1,000 cells counted in culture from each donor. □, G13; ▪, I10. C: Immunoblotting for PARP in protein extracted from islet cells following infection with nontarget (lane 3) or HES1 shRNA TRCN18993 virus (lane 4). Uninfected cells incubated with (lane 1) or without (lane 2) the apoptotic agent staurosporin served as controls. The lower band in lane 1 represents cleaved PARP. β-Actin served as a loading control. D: qPCR analysis of RNA extracted from islet cells following infection with HES1 shRNA TRCN18993 or nontarget virus. RQ indicates relative quantification compared with P0. Data are means ± SD (n = 3 donors). Only the change in p57 is significant (P = 0.001 vs. cells infected with nontarget virus, indicated by star). ▪, P0; □, nontarget;, HES1 shRNA. All the analyses were done 14 days following viral infection.